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Biomedical subjects

K Ohta

Publications and source records attributed to K Ohta.

At least 757 records · Page 42Linked to original sources
PubMed1986

[Toxicity studies of VP 16-213 (III)--Oral six-month chronic toxicity in rats].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered orally to Crj : CD (Sprague-Dawley) rats of both sexes at dose levels of 1, 3, 10 and 30 mg/kg/day for six months with the object of examining its chronic toxicity and the reversibility of toxic effects. The summarized results obtained are as follows: VP 30 mg/kg suppressed body weight increase and feed intake, and brought transient diarrhea, anemia and depilation. Some animals receiving this dose died showing systemic debility, emaciation and ataxia. VP 3 mg/kg and higher predominantly decreased red blood cell count as well as white blood cell count accompanied with lowered lymphocyte fraction. VP 30 mg/kg lowered total serum protein content and elevated A/G ratio in males, and lowered serum alkaline phosphatase activity in females. VP 10 and 30 mg/kg predominantly induced thymic atrophy, testicular atrophy with suppression of spermatogenesis and tubular atrophy, a decrease in epididymal weight, and splenic erythropoiesis. Above-described changes excluding the findings on testis and epididymis in VP 30 mg/kg group were shown to be generally reversible. Based on these results, the non-effect dose level of VP under the present experimental condition was estimated to be 1 mg/kg/day against rats of both sexes.

Administration, Oral↗
PubMed1986

[Toxicity studies of VP 16-213 (IV)--Intravenous one-month subacute toxicity in rats].

VP 16-213 (etoposide, abbr. to VP), an oncostatic drug, was administered intravenously to Crj : CD (Sprague-Dawley) rats of both sexes at dose levels of 0.15, 0.50, 1.5 and 4.5 mg/kg/day for one month with the object of examining its subacute toxicity and the reversibility of toxic effects. For the purpose of comparison, vincristine (abbr. to VCR) was administered in the same manner at dose levels of 0.04 and 0.08 mg/kg/day. The summarized results obtained are as follows: VP 0.50 mg/kg and higher suppressed body weight increase and food intake dose-responsively. VP 4.5 mg/kg brought depilation and anemia, and some of male animals receiving this dose died showing systemic debility, emaciation and ataxia. VP 0.50 mg/kg and higher decreased white blood cell count accompanied with lowered lymphocyte fraction, and 1.5 and 4.5 mg/kg predominantly decreased red blood cell count. VP 1.5 and 4.5 mg/kg lowered total serum protein content and serum alkaline phosphatase activity, and elevated A/G ratio. VP 0.50 mg/kg and higher predominantly decreased testicular weight, and 1.5 and 4.5 mg/kg predominantly brought thymic atrophy, hypoplasia of bone marrow and testicular atrophy with suppression of spermatogenesis and tubular atrophy. VP 4.5 mg/kg induced atrophy of germinal centers and hemosiderosis in spleen, and epididymal atrophy with decrease of sperms in number and appearance of giant cells. Above-described changes excluding the findings on testis and epididymis were generally reversible. Most of the findings for a reference drug, VCR, were similar to those for VP, and their severities brought by VP 1.5 and 4.5 mg/kg were comparable to those by VCR 0.04 and 0.08 mg/kg, respectively. Based on these results, the non-effect dose level of VP under the present experimental condition was estimated to be 0.15 mg/kg/day against rats of both sexes.

Anemia↗
PubMed1986

[A case of cholangiocarcinoma and dysgerminoma associated with Turner's syndrome].

A rare case of cholangiocarcinoma and dysgerminoma synchronously associated with Turner's syndrome was reported. A 53-year-old woman was admitted to our hospital on July 12, 1984 due to intrahepatic and left inguinal tumors. Physical examination revealed the typical characteristics of Turner's syndrome. The karyotype from myelocyte and fibrocyte culture was interpreted as 45, X. The resected intrahepatic tumor was cholangiocarcinoma that had invaded to the transverse mesocolon and the duodenum, while the inguinal lesion was dysgerminoma derived from a dysgenetic gonad. As far as we have been able to ascertain through our investigations of the literature on malignant disease in Turner's syndrome, the association of cholangiocarcinoma with Turner's syndrome has not been reported previously.

Adenoma, Bile Duct↗
PubMed1986

[Evaluation of computerized tomography-guided stereotactic evacuation of putaminal hematomas by somatosensory evoked potentials].

Computerized tomography (CT) guided stereotactic evacuation of intracerebral hematomas is effective and little invasive treatment at subacute or chronic stage. Somatosensory evoked potentials (SEPs) of 23 patients with putaminal hemorrhage whose stereotactic evacuations were performed from day 4 to day 24 are studied about surgical result and CT findings. As for SEP, N20 which is thought to be generated in the thalamus or in the primary parietal area receiving direct projections from the thalamus is used for comparison with functional recovery. Among 12 patients whose N20s before the evacuation showed normal, 9 had good recovery of their hemiplegia. Motor recovery tended to begin quickly after the evacuation and the evacuation of hematomas were thought to make better result than conservative treatment. CT findings of 9 patients with good recovery revealed that the hematomas didn't invade to the internal capsule or invaded to the posterior part of the posterior limb alone. Among 3 patients whose N20s before the evacuation were not distinct and those after the evacuation were normal, 2 had good recovery of their hemiplegia. As those hematomas were relatively large but located laterally, the internal capsule was seem to be not invaded but only compressed. Among 8 patients whose N20s were not distinct both before and after the evacuation, 7 could not get the recovery of their hemiplegia. CT findings of them revealed that the hematomas were large or invaded toward the internal capsule and thalamus. From this study N20s of SEPs are thought to be useful to the decision of indication and the prediction of the functional prognosis about stereotactic evacuation of putaminal hemorrhage.

Adult↗
PubMed1986

[Phase II study of mitoxantrone in patients with acute leukemia].

A phase II study of acute leukemia with mitoxantrone (MIT) was conducted by the Tokai Blood Cancer Study Group. The drug efficacy was evaluable in 31 cases (14 of ALL and 17 of ANLL) out of 37 entered at 13 institutions. Five cases were for first induction remission and 26 cases for re-induction remission; ages ranged from 7 to 69 (median: 43); 18 males and 13 females. MIT dosage was intravenous injection of 3-6 mg/m2/day X 5 consecutive days as a rule. Of the 14 cases of ALL, 2 achieved CR and 3, PR; the efficacy rate was 36%. Of the 17 cases of ANLL, 4 achieved CR and 3, PR: the efficacy rate was 41%. Of the 5 first induction remission cases, 3 achieved CR, and 1, PR, the efficacy rate being 80%, whereas out of the 26 re-induction remission cases, 3 achieved CR, 5 PR, and the efficacy rate was 31%. In 3 of 6 cases of CR, large cumulative doses of anthracyclines such as DNR 140 mg plus ACR 410 mg, DNR 360 mg plus ADR 120 mg plus ADR 120 mg, and DNR 240 mg plus ADR 540 mg, had been administered previously in each case. As to complications, sepsis and other infections were observed at the rates of 15% and 32%, respectively, from which it was inferred that in therapy with mitoxantrone, leukopenia should be observed carefully. The major non-hematological toxicity was gastrointestinal symptoms, but the degree was mild. From the results of this trial, it was concluded that mitoxantrone was an effective form of therapy for acute leukemia. Further clinical trials on mitoxantrone in combination with other drugs are scheduled.

Acute Disease↗
PubMed1986

[A phase II study of mitoxantrone in refractory and relapsed malignant lymphomas. Cooperative Study Group of Mitoxantrone in Malignant Lymphomas].

A phase II clinical trial of mitoxantrone in refractory or relapsed malignant lymphomas was conducted by a cooperative study involving 17 institutions. Of 46 patients entered, 33 were evaluable for responses and toxicity. Thirty-one of the 33 had been previously exposed to adriamycin at a median dose of 220 mg/m2 (range 21-489 mg/m2), and two additional patients had each been given THP-adriamycin at a dose of 80 mg/m2 or 4'-epi adriamycin at a dose of 69 mg/m2. Mitoxantrone was administered in 3 different schedules: 8-12 mg/m2, every 3-4 weeks in 23 patients; 4-6 mg/m2, weekly, in 3 patients; and 2-4 mg/m2, for 5 days, in 7 patients. Summarizing the responses obtained in the 3 schedules, there were 2 partial responders among 5 with Hodgkin's disease, while there were 8 complete responders and 4 partial responders among 28 with non-Hodgkin's lymphoma. The overall response rate for all the evaluable patients was 42% with a complete response rate of 24%. The median response duration was 7+ weeks (range 4-27+ weeks) for complete responders and 7 weeks (range 4-46+ weeks) for partial responders. The major toxicity was myelosuppression: leukocytopenia less than 3,000/microliter occurred in 79% of patients, and thrombocytopenia less than 75,000/microliter in 35%. Other toxic effects were minimal, mild nausea and/or vomiting occurred in 39%, and diarrhea in 3%. Possible drug-related liver and renal dysfunctions were observed in 19% and 10%, respectively. The favorable response to mitoxantrone in patients with prior anthracycline antibiotic therapy suggests that the drug is not fully cross-resistant with anthracycline antibiotics, and that this drug is of value in combination with other drugs as a salvage therapy for patients with refractory or relapsed malignant lymphomas.

Adolescent↗
PubMed1986

[Carnitine deficiency: a treatable cardiomyopathy].

This is a report of two brothers, six and five years of age, with systemic carnitine deficiency and cardiomyopathy, whose symptoms were improved after oral administrations of DL-carnitine. They had had progressive muscle weakness since three years of age. The elder brother's radiograph on admission showed cardiomegaly with a cardiothoracic ratio of 60%, and his electrocardiogram showed left ventricular hypertrophy and tall, peaked T waves in the precordial leads. The echocardiogram showed slight thickening of the cardiac muscle and decreased ejection fraction. Skeletal muscle biopsy specimens and sera were assessed for carnitine content. The skeletal muscle specimens revealed lipid storage myopathy, and the carnitine contents of the skeletal muscle and sera were both decreased. Myocardial biopsy for the elder brother revealed mitochondrial accumulation. Cardiomyopathy caused by carnitine deficiency is often fatal, but may be cured. Carnitine deficiency should be considered whenever a patient with cardiomegaly and progressive skeletal muscle weakness is encountered.

Cardiomyopathies↗